Understanding Drug Therapy for Non-Small Cell Lung Cancer

Running head: DRUG THERAPY
DRUG THERAPY
Name of Student:
Name of University:
Author’s Note:

1DRUG THERAPY
Answer no 1.
Lung cancer is the leading cause of cancer-related death. Non-small cell lungs comprise
approx. 85 % of all cancer. Non-small cell lung cancer is the type of epithelial lung cancer,
which constitute a various type of small bronchogenic carcinoma. (Davidson et al. 2016). It is
divided into three subtypes; they are adenocarcinoma, squamous cell carcinoma, and large cell
carcinoma. The different type of NSCLC develop in different location of lungs
Adenocarcinoma- It develops in lung periphery and alveolar type II cells
Squamous cell carcinoma- It starts in the cells of the central lung area and Mucociliary
epithelial cells.
Large cell carcinoma- develops in the central and peripheral lung area
The major risk factor for NSCLC includes smoking (85%), second-hand smoking, and
diet deficient in vitamin C (Gazda & Zhou 2018). According to current views on carcinogenesis
of NSCLC, the transformation of normal lung cell to malignant cell require culmination of
multiple and epigenetic alterations. It is believed that earlier alternation is caused by point
mutation and chromosomal deletion of tumor suppressor genes. Loss of function of TSG mainly
p53 causes 80% NSCLC of cases. TSG function in regulating cell cycle arrest, DNA repair, and
apoptosis. Mutation in p53 hinder its normal tumor suppressor capabilities; thus, DNA damage
remain unchecked, faulty cell proceed to cell cycle, and apoptosis is evaded (Tsakonas & Ekman
2018). This creates a situation where cell becomes more susceptible to further mutation. Another
critical alternation that results in the development of NSCLC is activation of oncogenes. In 50 to
90% NSCLC cases, EGFR oncogene is unregulated. The binding of EGF gene activates
signaling cascades that modulate transcription of a gene important in cell proliferation and

2DRUG THERAPY
resistance to apoptosis. In the majority of lung cancer, the activation of telomerase is detected
(Marien et al. 2015). Telomerase is hexameric nucleotide repeats that protect the end of the
chromosome from separating. It shortens with each cell division, limited cell proliferation
(Furtado et al. 2015). However, by polymerization of telomerase can contribute to prolonging
cell survival. The malignant cell proliferates and escapes programmed cell death. The lung tumor
makes ups the fluid that builds in the lungs spaces that surround it.
Further, it pushes the air out of the lungs and results in the collapse of the lungs. Due to
this, oxygen is unable to get into the lungs, and passage of carbon dioxide from the lungs is
blocked. This causes difficulty in breathing or shortness of breath.
NSCLC spread to other body parts by the process known as metastasis (Vizoso et al.
2015). It metastases through tissue, lymph, and blood. It spread to a different location in the
lungs causes various type of NSCLC. In order to metastases, tumor cell requires adequate blood
supplies and consequently promotes angiogenesis by producing VEGF. It binds to VEGF
receptor present in epithelial cells of the lungs and leads to the formation of new blood vessels as
NSCLC advances it metastases to another area of lungs and other organs like brain, liver, and
bones.
Answer no 2.
The chemotherapy medication is the combination of drug given to the cancer patients,
which reflects that the patient receives more than two medicines at the same time (Phillips et al.
2016). The pharmacokinetics of the drugs given to Nigel for the treatment of secondary liver
cancer helps to understand its metabolism and how body causes changes in medications which
explains its analysis, distribution, metabolism, and excretion.

3DRUG THERAPY
It helps to understand the route of administration and concentration of dose that should
be given to the treatment. As Nigel is having secondary liver cancer, the current medication
given to him is Cisplatin and Docetaxel, which is used for adjuvant therapy. They are known to
treat various malignancies and limit the spread of cancerous cells (Kinoshita et al. 2015). This
drug can be administered both intravenously and orally.
The absorption of Cisplatin and Docetaxel drugs depends on their bioavailability. The
drug given to the patient is through intravenous mode, which has to increase its variability
because it has undergone the process of being transported across the intestine and then passes to
the liver and then enter the systematic plasma circulation (Shukuya et al. 2015). These steps are
known as pharmacokinetic, which involve the absorption, first pass metabolism, and its
elimination before entering the circulation pathway.
The metabolism of the drug given to the patient undergoes hepatic first pass pathways
(Zhang et al. 2019). Metabolism occurs in the liver as the drug is semi-synthetic taxane, which
gets excreted through feces (Sohail et al. 2018). The drugs get demethylated by the cytochrome
P450 3A subfamily, which includes CYP3A4 and CYP3A5. CYP34A are involved in a greater
extent and CYP3A5 lo less extent. Apart from this, CYP1A2 is intricate as a minor enzymatic
component in the process of metabolism. The metabolism is mainly caused oxidation reaction in
the side chain of tert-butylpropionate and result in alcohol docetaxel M2. The metabolite of drug
are formed by cyclisation of M2 and form M3, M1 M4 (Nieuweboer et al. 2015).
The drug then passes through the apical membrane of enterocyte. The ABC transporter
mainly ABCB1 and ABCC2 are involved in the intestinal first pass metabolism by the
metabolizing enzyme. They causes efflux of some part of drug back to intestine and some part of
the drug are absorbed into the mesenteric blood circulation and then it enters the liver through